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Intestinal Metaplasia and Dysplasia

Intestinal metaplasia (IM) can be subdivided into 3 categories, as classified by Filipe’s group.199Type I (complete) IM contains goblet cells that secrete sialomucins and mature, nonsecretory absorptive cells. Type 1 IM is not a risk factor for gastric cancer. Type II (incomplete) IM contains few if any absorptive cells, columnar “intermediate” cells in various stages of differentiation secreting neutral or acidic sialomucins, and goblet cells secreting sialomucins and/or occasionally sulfomucins. Type III (incomplete) is less differentiated than type II, with the intermediate cells secreting mainly sulfomucins and the goblet cells secreting sialo- and/or sulfomu- cins. Type II or III IM is associated with an approximately 20-fold increased risk of gastric cancer.200,201 Early gastric cancer develops in 42% of patients with type III IM within 5 years of follow-up, suggesting that IM represents a precursor lesion for the intestinal form of gastric cancer.201 However, whether cancer arises from areas of IM or whether IM simply represents a marker for higher gastric cancer risk remains unclear. As is the case with atrophic gastritis, the prevalence of IM in Hp-infected individuals is higher in Asia (≈40%) as compared to the West.193,194

As mentioned earlier, a number of recent studies have revealed that intestinal metaplasia is not the only possible metaplastic precursor of gastric cancer. While controversy exists as to the sequence and connection of mucosal lineage changes associated with increased risk for gastric cancer, there is a general agreement that the loss of acid secreting parietal cells, also known as oxyntic atrophy, is a prerequisite for induction of metaplasia. Antralization of the fundus, or the presence of metaplastic glands in the fundus with a general phenotype similar to that of the antral or pyloric glands (also known as pseudopyloric metaplasia), is frequently associated with intestinal type adenocarcinoma. This phenotype has also been called spasmolytic polypeptide-expressing metaplasia (SPEM)202 and is characterized by the presence of trefoil factor 2 (TFF2, or spasmolytic polypeptide) immunoreactive cells in the gastric fundus, with morphologic characteristics similar to those of deep antral gland cells. SPEM was observed in association with over 90% of resected gastric cancers in 3 studies in the United States, Japan, and Iceland.202-204 SPEM and intestinal metaplasia might share equal importance as putative preneoplastic lesions in the stomach. Nevertheless, it remains to be determined whether either or both of these metaplasias can progress to dysplasia or neoplasia. Alternatively, intestinal metaplasia may potentially reflect a further benign attempt by the mucosa to increase repair in the face of chronic infection and inflammation.

Histologic assessment of gastric dysplasia and adenocarcinoma is based on the Vienna classification, the result of an international consensus conference of GI pathologists in 2000 (Table 54-3).205 The prevalence of gastric dysplasia ranges from as low as 0.5% in low-risk areas206 to 20% in high-risk areas.207 Prospective studies have shown that low-grade dysplasia may regress in up to 60% of cases, whereas 10% to 20% progress to high-grade dysplasia (Fig. 54-4).208-210 High-grade dysplasia rarely regresses, and is associated with a 2% to 6% annual incidence of progression to gastric cancer.210-212 In Histologic assessment of gastric dysplasia and adenocarcinoma is based on the Vienna classification, the result of an international consensus conference of GI pathologists in 2000 (Table 54-3).205 The prevalence of gastric dysplasia ranges from as low as 0.5% in low-risk areas206 to 20% in high-risk areas.207 Prospective studies have shown that low-grade dysplasia may regress in up to 60% of cases, whereas 10% to 20% progress to high-grade dysplasia (Fig. 54-4).208-210 High-grade dysplasia rarely regresses, and is associated with a 2% to 6% annual incidence of progression to gastric cancer.210-212 In a prospective cohort study from the Netherlands, the presence of high-grade dysplasia was associated with a 40-fold increased risk of progression to gastric cancer.211 High-grade dysplasia is often associated with synchronous cancer and can be uni- or multifocal.213